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warnings
WARNINGS Anaphylactoid and Possibly Related Reactions Presumably because angiotensin-converting inhibitors affect the metabolism of eicosanoids andpolypeptides, including endogenous bradykinin, patients receiving ACE inhibitors (including quinapril hydrochloride) may be subject to a variety of adverse reactions, some of them serious. Head and Neck Angioedema Angioedema of the face, extremities, lips, tongue, glottis, and larynxhas been reported in patients treated with ACE inhibitors and has been seen in 0.1% of patientsreceiving quinapril hydrochloride. In two similarly sized U.S. postmarketing trials that, combined, enrolled over 3,000 black patients andover 19,000 non-blacks, angioedema was reported in 0.30% and 0.55% of blacks (in study 1 and 2respectively) and 0.39% and 0.17% of non-blacks. Angioedema associated with laryngeal edema can be fatal. If laryngeal stridor or angioedema of theface, tongue, or glottis occurs, treatment with quinapril hydrochloride should be discontinuedimmediately, the patient treated in accordance with accepted medical care, and carefully observeduntil the swelling disappears. In instances where swelling is confined to the face and lips, thecondition generally resolves without treatment; antihistamines may be useful in relieving symptoms. Where there is involvement of the tongue, glottis, or larynx likely to cause airway obstruction,emergency therapy including, but not limited to, subcutaneous epinephrine solution 1:1000(0.3 to 0.5 mL) should be promptly administered (see ADVERSE REACTIONS ). Intestinal Angioedema Intestinal angioedema has been reported in patients treated with ACEinhibitors. These patients presented with abdominal pain (with or without nausea or vomiting); insome cases there was no prior history of facial angioedema and C-1 esterase levels were normal.The angioedema was diagnosed by procedures including abdominal CT scan or ultrasound, or atsurgery, and symptoms resolved after stopping the ACE inhibitor. Intestinal angioedema should beincluded in the differential diagnosis of patients on ACE inhibitors presenting with abdominal pain. Patients with a history of angioedema Patients with a history of angioedema unrelated to ACEinhibitor therapy may be at increased risk of angioedema while receiving an ACE inhibitor (see also CONTRAINDICATIONS ). Anaphylactoid reactions during desensitization Two patients undergoing desensitizingtreatment with hymenoptera venom while receiving ACE inhibitors sustained life-threateninganaphylactoid reactions. In the same patients, these reactions were avoided when ACE inhibitorswere temporarily withheld, but they reappeared upon inadvertent rechallenge. Anaphylactoid reactions during membrane exposure Anaphylactoid reactions have beenreported in patients dialyzed with high-flux membranes and treated concomitantly with an ACEinhibitor. Anaphylactoid reactions have also been reported in patients undergoing low-densitylipoprotein apheresis with dextran sulfate absorption. Hepatic Failure Rarely, ACE inhibitors have been associated with a syndrome that starts withcholestatic jaundice and progresses to fulminant hepatic necrosis and (sometimes) death. Themechanism of this syndrome is not understood. Patients receiving ACE inhibitors who developjaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receiveappropriate medical follow-up. Hypotension Excessive hypotension is rare in patients with uncomplicated hypertension treatedwith quinapril hydrochloride alone. Patients with heart failure given quinapril hydrochloride commonlyhave some reduction in blood pressure, but discontinuation of therapy because of continuingsymptomatic hypotension usually is not necessary when dosing instructions are followed. Cautionshould be observed when initiating therapy in patients with heart failure (see DOSAGE ANDADMINISTRATION ). In controlled studies, syncope was observed in 0.4% of patients (N=3203); thisincidence was similar to that observed for captopril (1 %) and enalapril (0.8%). Patients at risk of excessive hypotension, sometimes associated with oliguria and/or progressiveazotemia, and rarely with acute renal failure and/or death, include patients with the followingconditions or characteristics: heart failure, hyponatremia, high dose diuretic therapy, recent intensivediuresis or increase in diuretic dose, renal dialysis, or severe volume and/or salt depletion of anyetiology. It may be advisable to eliminate the diuretic (except in patients with heart failure), reducethe diuretic dose or cautiously increase salt intake (except in patients with heart failure) beforeinitiating therapy with quinapril hydrochloride in patients at risk for excessive hypotension who areable to tolerate such adjustments. In patients at risk of excessive hypotension, therapy with quinapril hydrochloride should be startedunder close medical supervision. Such patients should be followed closely for the first two weeks oftreatment and whenever the dose of quinapril hydrochloride and/or diuretic is increased. Similarconsiderations may apply to patients with ischemic heart or cerebrovascular disease in whom anexcessive fall in blood pressure could result in a myocardial infarction or a cerebrovascular accident. If excessive hypotension occurs, the patient should be placed in the supine position and, ifnecessary, receive an intravenous infusion of normal saline. A transient hypotensive response is nota contraindication to further doses of quinapril hydrochloride, which usually can be given withoutdifficulty once the blood pressure has stabilized. If symptomatic hypotension develops, a dosereduction or discontinuation of quinapril hydrochloride or concomitant diuretic may be necessary. Neutropenia/Agranulocytosis Another ACE inhibitor, captopril, has been shown to causeagranulocytosis and bone marrow depression rarely in patients with uncomplicated hypertension,but more frequently in patients with renal impairment, especially if they also have a collagen vasculardisease, such as systemic lupus erythematosus or scleroderma. Agranulocytosis did occur duringquinapril hydrochloride treatment in one patient with a history of neutropenia during previouscaptopril therapy. Available data from clinical trials of quinapril hydrochloride are insufficient to showthat, in patients without prior reactions to other ACE inhibitors, quinapril hydrochloride does notcause agranulocytosis at similar rates. As with other ACE inhibitors, periodic monitoring of whiteblood cell counts in patients with collagen vascular disease and/or renal disease should beconsidered. Fetal/Neonatal Morbidity and Mortality ACE inhibitors can cause fetal and neonatal morbidity anddeath when administered to pregnant women. Several dozen cases have been reported in the worldliterature. When pregnancy is detected, ACE inhibitors should be discontinued as soon as possible. The use of ACE inhibitors during the second and third trimesters of pregnancy has been associatedwith fetal and neonatal injury, including hypotension, neonatal skull hypoplasia, anuria, reversible orirreversible renal failure, and death. Oligohydramnios has also been reported, presumably resultingfrom decreased fetal renal function; oligohydramnios in this setting has been associated with fetallimb contractures, craniofacial deformation, and hypoplastic lung development. Prematurity,intrauterine growth retardation, and patent ductus arteriosus have also been reported, although it isnot clear whether these occurrences were due to the ACE inhibitor exposure. These adverse effects do not appear to have resulted from intrauterine ACE inhibitor exposure thathas been limited to the first trimester. Mothers whose embryos and fetuses are exposed to ACEinhibitors only during the first trimester should be so informed. Nonetheless, when patients becomepregnant, physicians should make every effort to discontinue the use of quinapril hydrochloride assoon as possible. Rarely (probably less often than once in every thousand pregnancies), no alternative to ACEinhibitors will be found. In these rare cases, the mothers should be apprised of the potential hazardsto their fetuses, and serial ultrasound examinations should be performed to assess the intraamnioticenvironment. If oligohydramnios is observed, quinapril hydrochloride should be discontinued unless it isconsidered lifesaving for the mother. Contraction stress testing (CST), a non-stress test (NST), orbiophysical profiling (BPP) may be appropriate, depending upon the week of pregnancy. Patientsand physicians should be aware, however, that oligohydramnios may not appear until after the fetushas sustained irreversible injury. Infants with histories of in utero exposure to ACE inhibitors should be closely observed forhypotension, oliguria, and hyperkalemia. If oliguria occurs, attention should be directed towardsupport of blood pressure and renal perfusion. Exchange transfusion or dialysis may be required asa means of reversing hypotension and/or substituting for disordered renal function. Removal ofquinapril hydrochloride, which crosses the placenta, from the neonatal circulation is not significantlyaccelerated by these means. No teratogenic effects of quinapril hydrochloride were seen in studies of pregnant rats and rabbits.On a mg/kg basis, the doses used were up to 180 times (in rats) and one time (in rabbits) themaximum recommended human dose.